China
Africa
Explore chapters and articles related to this topic
Articular Cartilage Pathology and Therapies
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
Not surprisingly, many of the candidate genes identified are those of the articular cartilage extracellular matrix. Candidate genes identified through familial studies are matrix genes such as COL2A1, COL1A1, cartilage oligomeric matrix protein (COMP), aggrecan (ACAN), matrilin 3 (MATN3), and asporin (ASPN) (Bleasel et al. 1999; Meulenbelt et al. 1999; Mustafa et al. 2000; Stefansson et al. 2003; Kizawa et al. 2005). However, more distantly associated genes involved in the development and maintenance of the joint have also been implicated (Sandell 2012).
Advances in Osteoarthritis of the Hip
Published in K. Mohan Iyer, Hip Joint in Adults: Advances and Developments, 2018
Pratham Surya, Sriram Srinivasan, Dipen K. Menon
OA is a disease with varied pathophysiology. A workshop on aetiopathogenesis of OA concluded that OA can be idiopathic (aetiology unknown). It was previously believed to be caused by wear and tear of the joint. Currently scientists and researchers believe it to be a disease of the joint. Some factors that have a role in development of hip OA are as follows:Genetic: OA has a significant heritable component. Genes associated with OA tend to be associated with the process of synovial joint development. Mutations in these genes might directly cause OA [9]. Early-age-onset OA is caused by mutations in matrix molecules often associated with chondrodysplasias. Middle-age onset of OA is caused by mutations that predispose the joint to injury or malalignment and late-age-onset OA to mutations that regulate subtle aspects of joint development and structure [9]. Some inherited traits may result in a rare defect where the body does not produce collagen, which is a component protein in cartilage. Recently, researchers found that a gene called FAAH (fatty acid amide hydrolase), which mediates pain, is found to be higher in patients suffering from OA than in a normal person [13]. Other genes that are linked to OA are vitamin D receptor, oestrogen receptor-1 and inflammatory cytokines such as IL-1, IL-4 and matrilin-3.Obesity: A high body mass index (BMI) increases the pressure on lower limb weight-bearing joints such as the hip and knee. It is also proven that an excess of fat tissue induces the production of inflammatory cytokines, which can cause further damage to the joints.Overuse and damage: Occupational hazards such prolonged weight bearing and heavy lifting can lead to damage of the cartilage. Intra-articular fractures lead to OA.Developmental or acquired deformities: Some examples are hip dysplasia, Perthes disease of the hip (Fig. 19.3) and slipped upper femoral epiphysis (SUFE).Joint disorders in athletes: Injuries involving a joint are very common in athletes. Joint injuries occur in professional players, especially soccer players. In every thousand hours on the sports field 10 to 35.5 injuries are reported [13]. Articular cartilage has very poor regenerative properties, leading to OA. A study conducted on soccer players indicates that 32%-49% of the players have OA. In a study it was determined that there is a threefold increased risk of hip OA in elite players than comparatively less elite ones [13].Other or miscellaneous factors: Hormonal disturbances, like an excess of growth hormone, lead to OA. Other joint and metabolic disorders may lead to an increased risk of OA.
Reconstructive rhinoplasty using cadaver cartilage in relapsing polychondritis
Published in Baylor University Medical Center Proceedings, 2023
Rishabh Shah, Eugene L. Alford
Accumulating data strongly suggest that both humoral and cell-mediated immunity play a role in the pathogenesis of relapsing polychondritis. Antibodies to type II collagen, matrilin-1, and immune complexes are detected in the serum of patients. The possibility that an immune response to type II collagen may be important in the pathogenesis has been supported in animal studies. Humoral responses to type IX and type XI collagen, matrilin-1 (noncollagenous protein present in the extracellular matrix in cartilage), and cartilage oligomeric matrix protein have been demonstrated in some patients. One study showed that rats immunized with matrilin-1 were found to develop severe inspiratory stridor and swelling of the nasal septum. The rats had severe inflammation with erosions of the involved cartilage, which was characterized by increased numbers of CD4+ and CD8+ T cells in the lesions. All had IgG antibodies to matrilin-1. A subsequent study demonstrated serum anti-matrillin-1 antibodies in ∼13% of patients with relapsing polychondritis. Cell-mediated immunity may also be operative in causing tissue injury, since lymphocyte transformation can be demonstrated when lymphocytes of patients are exposed to cartilage extracts. T cells specific for type II collagen have been found in some patients, and CD4+ T cells have been observed at sites of cartilage inflammation.2
Relapsing polychondritis: state-of-the-art review with three case presentations
Published in Postgraduate Medicine, 2021
Bogna Grygiel-Górniak, Hamza Tariq, Jacob Mitchell, Azad Mohammed, Włodzimierz Samborski
Autoantibodies directed against cartilage matrix components are also focal in the pathophysiology of RPC. Autoantibodies against collagen type II are encountered in an acute flare of RPC. Anti-collagen type IX and XI antibodies are other markers that have been identified; however, their specific function needs to be established [16,18]. An anti-matrilin-1 autoantibody is of considerable interest, as it was seemingly reproducing the disease when administered against matrilin-1 in animal models. Matrilin-1 is an extracellular matrix protein found mainly in tracheal cartilage, and its level substantially rises during the disease’s respiratory flares. Nevertheless, the mentioned autoantibodies are neither specific nor sensitive to RPC, decreasing their pathogenic value [16,19,20].